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Blood, 1 May 2006, Vol. 107, No. 9, pp. 3486-3488.
Prepublished online as a Blood First Edition Paper on January 17, 2006; DOI 10.1182/blood-2005-08-3319.
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Submitted August 16, 2005
Accepted November 28, 2005
High levels of circulating CD34 cells, dacrocytes, clonal hematopoiesis, and JAK 2 mutation differentiate myelofibrosis with myeloid metaplasia from secondary myelofibrosis associated with pulmonary hypertension
Uday Popat, Adaani Frost, Enli Liu, Yongli Guan, April Durette, Reddy Vishnu, and Josef T Prchal*
Divisions of Hematology/Oncology, Center for Cell and Gene Therapy, and Division of Pulmonary Medicine, Baylor College of Medicine, Houston, TX, USA; Department of Blood and Marrow Transplantation, The University of Texas MD Anderson Cancer Center, Houston, TX, USA
Divisions of Hematology/Oncology, Center for Cell and Gene Therapy, and Division of Pulmonary Medicine, Baylor College of Medicine, Houston, TX, USA
Department of Pathology, University of Alabama, Birmingham, AL, USA
Divisions of Hematology/Oncology, Center for Cell and Gene Therapy, and Division of Pulmonary Medicine, Baylor College of Medicine, Houston, TX, USA; Department of Pathophysiology, First School of Medicine Charles University, Prague, Czech Republic
* Corresponding author; email: jprchal{at}bcm.tmc.edu.
We studied 25 patients with myelofibrosis with myeloid metaplasia and 19 patients with secondary myelofibrosis associated with pulmonary hypertension. In these two groups, we compared the peripheral blood CD34 count, the clonality of granulocytes and platelets in peripheral blood, the mutational status of the JAK 2-kinase gene, and the morphology of the peripheral blood and bone marrow. We found that the following were distinctive features of myelofibrosis with myeloid metaplasia but not of secondary myelofibrosis due to PH: high circulating CD34 cell count, the presence of clonal platelets and granulocytes and of peripheral blood dacrocytes, and a JAK2 1849G >T (V617F) mutation. We conclude that these are intrinsic features of clonal progenitors present in patients with myelofibrosis due to myeloproliferative disorders and that these features are not due to the abnormal marrow architecture seen in secondary myelofibrosis.
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